Common widely used vaccines are made from pathogens (e.g., microorganisms, viruses) or such pathogens whose toxicity is partially weakened or eliminated. The vaccines are administered to living bodies to induce immunity to prevent infectious diseases.
Dendritic cells after having engulfed viruses, microorganisms, or like foreign bodies migrate to lymph nodes and give naive T cells (Th0 cells) the information of the foreign bodies, thus inducing the differentiation of helper T cells. Through the interaction with dendritic cells, Th0 cells differentiate into type 1 helper T cells (Th1 cells), which are responsible for cellular immunity, and type 2 helper T cells (Th2 cells), which are responsible for humoral immunity (see Non-Patent Literature 1 and Non-Patent Literature 2, for example).
Many toll-like receptors (TLRs) are expressed in immunocompetent cells responsible for the innate immunity system, including dendritic cells. They are activated upon receiving a TLR ligand and promote the differentiation of helper T cells, thus activating immune reactions (see Non-Patent Literature 3, for example). For immunity activation, only the reaction routes via TLRs have been known, and other reaction routes have remained unclear.
It is known that immunity activation effects can be given by toxins such as cholera toxin or Escherichia coli heat-labile enterotoxin or fat/oil adjuvants that enhance the effects of immune reactions by slow-release of antigens. However, they have problems in terms of the balance between the safety and the efficacy (see Non-Patent Literature 4, for example).
It is also known that a trypsin-like serine protease called thrombin, which is responsible for forming hemostatic plugs or healing of wounds, is involved with immune response and used as an adjuvant for promoting antibody production (see Patent Literature 1, for example).
It is unknown, however, if thrombosis treatment drugs (e.g., anticoagulants that inhibits blood coagulation factors, antiplatelets that inhibits aggregation of platelets) with effects opposite to those of thrombin, which is responsible for thrombus formation, can be effectively used as an adjuvant for promoting antibody production. It is also unknown if direct administration of the thrombosis treatment drug with an antigen to a living body can induce an antigen-specific humoral immune response.